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• 基础研究 • 上一篇    下一篇

东亚钳蝎蝎毒多肽组分Ⅲ对肝癌细胞凋亡的影响

李建伟1,胡 静2,张桂荣1,魏征人3*   

  1. 1. 吉林大学基础医学院生物化学与分子生物学实验中心,吉林 长春 130021;2. 吉林大学第二医院妇产科,吉林 长春130041;3. 吉林大学基础医学院药理学教研室,吉林 长春 130021
  • 收稿日期:2005-09-29 修回日期:1900-01-01 出版日期:2006-07-28 发布日期:2006-07-28
  • 通讯作者: 魏征人

Effects of anti-cancer peptide fraction Ⅲ from Buthus Martensii Karsch on apoptosis of human liver cancer cells

LI Jian-wei1, HU Jing2,ZHANG Gui-rong1,WEI Zheng-ren3*   

  1. 1. Experimental Center of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Jilin University, Changchun 130021, China;2. Department of Obstetrics and Gynecology, Second Hospital, Jilin University, Changchun 130041, China;3. Department of Pharmacology, School of Basic Medical Sciences,Jilin University, Changchun 130021, China
  • Received:2005-09-29 Revised:1900-01-01 Online:2006-07-28 Published:2006-07-28
  • Contact: WEI Zheng-ren

摘要: 目的:探讨东亚钳蝎蝎毒多肽组分Ⅲ对肝癌细胞凋亡的影响及其诱导凋亡的初步机制。 方法:将人肝癌细胞株Hep G2浸润在不同浓度的蝎毒多肽组分Ⅲ溶液中,应用DNA凋亡梯状带分析法和DNA末端转移酶介导的末端标记法(TUNEL法)测定凋亡的发生及凋亡率;用Western blotting方法观察Bcl-2蛋白和Caspase-3的表达量。 结果:蝎毒多肽组分Ⅲ引起的肝癌细胞株Hep G2凋亡呈剂量依赖性变化。DNA凋亡呈现明显的梯状带电泳行为。经5、10、50、100及200 mg·L-1蝎毒多肽组分Ⅲ处理12 h 后,肝癌细胞凋亡率分别为(6.1±3.0)%、(15.3±4.9)%、(48.5±5.2)%、(66.7±6.5)%和(91.2±6.9)%。凋亡伴随着bcl-2基因的表达下调,在凋亡过程中Caspase -3被激活。 结论:东亚钳蝎蝎毒多肽组分Ⅲ可以促进人肝癌细胞株Hep G2的凋亡,并且这种凋亡可能与通过下调bcl-2基因和激活Caspase-3途径有关。

关键词: 细胞凋亡, Bcl-2, Caspase-3, 肝肿瘤

Abstract: Objective To study the inhibitory effect of anti-cancer peptide fraction Ⅲ from crew scorpion venom of Buthus Martensii Karsch on apoptosis of Hep G2 liver cancer cells and its mechanism. Methods Human Hep G2 liver cancer cells were treated with various concentrations of scorpion venom fraction Ⅲ for different durations. Apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated nick end-labeling (TUNEL) and DNA fragmentation assays. Caspase-3 and proteins of Bcl-2 family were assayed by Western blotting. Results Anti-cancer peptide fraction Ⅲ induced endothelial apoptosis in a dose-dependent manner. After treatment for 12 h, in scorpin venom fraction Ⅲ groups with different concentrations of 5, 10, 50, 100, 200 mg·L-1, the apoptotic rates were (6.1±3.0)%, (15.3±4.9)%, (48.5±5.2)%, (66.7±6.5)% and (91.2±6.9)%, respectively. The apoptosis was accompanied by down-regulation of Bcl-2 protein synthesis. Caspase-3 was activated during apoptosis. Conclusion The anti-cancer peptide fraction Ⅲ can induce apoptosis in human Hep G2 liver cancer cells through down-regulation of Bcl-2 protein and activation of Caspase-3 pathways.

Key words: apoptosis, Bcl-2, Caspase-3, liver neoplasms

中图分类号: 

  • R282.74